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Related Experiment Video

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Aspirin-another caloric-restriction mimetic.

Federico Pietrocola1,2,3,4,5, Francesca Castoldi1,2,3,4,5,6,7, Maria Chiara Maiuri1,2,3,4,5

  • 1a Gustave Roussy Cancer Campus , Villejuif , France.

Autophagy
|June 23, 2018
PubMed
Summary

Aspirin and its metabolite salicylate promote autophagy, a cellular process that may slow aging. This action is achieved by inhibiting EP300, making aspirin a caloric-restriction mimetic.

Keywords:
AMPKAcetylationagingautophagyfastinginflammationlongevitymitophagysalicylate

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Area of Science:

  • Biogerontology
  • Cellular Biology
  • Pharmacology

Background:

  • Cellular fitness and adaptation decline with age due to environmental and genetic insults.
  • Macroautophagy/autophagy is crucial for maintaining cellular fitness and health span.
  • Caloric restriction (CR) counteracts aging but is difficult for humans; caloric-restriction mimetics (CRMs) offer an alternative.

Purpose of the Study:

  • To investigate if aspirin and its metabolite salicylate can induce autophagy.
  • To determine the mechanism by which aspirin and salicylate affect autophagy.
  • To establish aspirin as a potential caloric-restriction mimetic.

Main Methods:

  • Investigated the effect of aspirin and salicylate on autophagic flux.
  • Examined the interaction between salicylate and the enzyme acetyltransferase EP300.
  • Tested aspirin's autophagy-inducing effects in mouse models and *Caenorhabditis elegans*.

Main Results:

  • Aspirin and salicylate were found to stimulate autophagic flux.
  • This stimulation occurs via inhibition of EP300 by salicylate, competing with acetyl coenzyme A.
  • The mechanism of action was conserved across different species, including mice and *C. elegans*.

Conclusions:

  • Aspirin, through its metabolite salicylate, acts as a caloric-restriction mimetic by inducing autophagy.
  • Inhibition of EP300 is the key mechanism for aspirin's autophagy-promoting effects.
  • Aspirin represents a potential therapeutic strategy for promoting health span and counteracting aging.